Major Non-glomerular Diseases Flashcards
what are non-glomerular diseases? where is the pathology taking place
what are the 3 Tubulointerstitial Diseases
- diseases which affect the tubules (PCT, LOH, DCT, etc.) & those which impact the parynchema
not focusing on the glomerulus here – just other kidney pathology
Tubulointerstitial Disease
- Acute Tubular Necrosis (ANT)
- Interstital Nephritis
- Chronic tubulointerstitial nephropathy
Acute Tubular Necrosis
- Etiology
most common tubulointerstital disease – aka intrinsic
Etiology
- can result from ischemia or can result from nephrontoxins
- a destruction of the tubules from (ischemic or toxin agents) which results in shedding cells & lack of flow –> necrosis of the tubules and reduced kidney function
Ischemic etiology
- prolonged hypotension: blood shunted away and not enough to perfuse the kidneys
- hypoxia: volume depeletion, shock, sepsis (shunting)
- post major surgical procedure
Nephrotoxic etiology
EXOgenous: coming from outside the body
- aminoglycosides
- amphotericin B
- vancomycin
- radio contrast!
- acyclovir
- celphalosporins
- cyclosporine
- heavy metals
ENDOgenous: coming from within the body creating toxic
- myoglobinuria: a result of muscle breakdown
- hemoglobin (hemolytic anemia)
- hyperuricemia
- Bence Jones Proteins (from multiple myloma)
ATN
Diganosis
Treatment
Diagnosis
most essentail is a urinalysis!!
- see muddy brown casts KEY of ATN because the epithelial cells are sluffing off and dying & flushed out into urine
- urine sodium concentration is elevated: because unable to reabsorb
- hyperkalemia (because AKI : metabolic acidosis)
- hyperphosphatemia
- BUN:Cr ratio is LOW (because the body is unable to reabsorb the BUN since the cells are damaged) less than 20:1
Treatment
- take away the offending agent if possible: then manage symptoms
- if fluid overlaoded: give diueretics
- avoid fluid overloading & increaseing the hyperkalemia remove meds and IV fluids (restrict)
- restrict protein: to stop the retention
- if needed: Dialysis (short term) to fix the electrolytes, volume, inc. uremia, or worsening acidosis
- most can and will resolve in 7-21 days
Interstitial Nephritis
Etiology
Presentation
Interstitial Nephritis: think inflammatory/allergic reaction happening in the kidneys
Etiology
- an inflammatory resposne which results in edema and potential to damange the tubules
medication etiology
- penicillins
- cephalosporins
- sulfonamides
- NSAIDS
- rifampin
- phenyotin
- allopurinal
- PPIs
Infectious Agents Etiology
- strep infections
- Rocky Mountian Spotted Fever
- CMV
- leptosporosis
- histoplasmosis
idopathic or other Etiology
- SLE
- Sjogrens
- sarcoidosis
- crygloobinemia
Presentation: essentially its a systemic inflammatory allergic reaction type which impacts the kidneys
- Fever
- Rash
- Arthralgias
- eosinophilila (in blood & can see in urine (PPP))
Interstital Nephritis
Diagnosis
Treatment
Diagnosis
Urinialysis
- RBCs
- WBCs
- white cell casts
- proteinuria
Treatment
- removal of the agent/med/NSAID/sulfa/PCN/PPI
- supportive care
- can consider corticosteroids
- dialysis may be needed (1/3 of) if no clinical improvement
Chronic Tubulointerstitial Nephropathy
Etiology
Presentation
Etiology (think obstrutive causes backlong of urine leading to damage) not due to an acute issue
most commony is a prolonged obstructive uropathy: something which leads to injury over time of the tubules
- BPH in men
- ureteral stone (within a single kidney pt.)
- bilateral ureteral stones
- carcinomas & cancers which obstruct the flow of urine
vesicoureteral reflux is second most common cuase
- a dx. for young kids (under 5) who have recurrent UTIs due to the floppy valves which hold urine within the bladder: they allow backflow and infections
- can be after a kidney transplant too
- US: shows renal scarring and hydronephrosis
other causes
- analgesics, metals, mesoamerican and balkan nephropathy
Chronic Tubulointerstitial Nephropathy
Etiology
Presentation
Etiology (think obstrutive causes backlong of urine leading to damage) not due to an acute issue
most commony is a prolonged obstructive uropathy: something which leads to injury over time of the tubules
- BPH in men
- ureteral stone (within a single kidney pt.)
- bilateral ureteral stones
- carcinomas & cancers which obstruct the flow of urine
vesicoureteral reflux is second most common cuase
- a dx. for young kids (under 5) who have recurrent UTIs due to the floppy valves which hold urine within the bladder: they allow backflow and infections
- can be after a kidney transplant too
- US: shows renal scarring and hydronephrosis
- staged: grade 5 = surgery, grade 1-3 usually self resolve, grade 4: prophylaxis abx. may be needed
other causes
- analgesics, metals, mesoamerican and balkan nephropathy
Chronic Tubulointerstital Nephropathy
Diagnosis
Treatment
Diagnosis
- US/CT/MRI may be needed to see the obstruction
- UA: bland, possible hematuria, pyuria or bacteruira
- can see polyuria or oligouria
- HTN and increase BUN (nitrogen in blood)
since its chronic… eventually…
- decreased GFR
- interstital fiberosis and tubular atrophy
- reduced kidney size
Treatment
- treat underlying cause/ remove agents
- treat the HTN assocaited with it
- treat the proteinuria
- ACE/ARBS help with both the above issues
Renal Artery Stenosis
Etiology
Presentation
Etiology
- majority are due to atherosclerosis in the proximal (ostial) portion of the arteries (one or both)
- Fibromuscular dysplasia: beading of the artery : several sites along the atery where the wall hypertrophies (not atherosclerosis) and it occludes flow
- fibromuscular: younger women (40s) & resistant or sudden spike in HTN & beads-on-string appearance on MRA imaging
Decreased renal blood flow: triggers the kidneys to think “hey, we need more pressure” & activates the RAAS system: HTN
Presentation: suspect when…
- new onset HTN before 20 or suddenly after 50
- combo of 3+ HTN meds arent controlling them
- renal artery bruits!
- pt. HAS peripheral arterial atherosclerosis (probably here too)
- initiation of an ACE sends them into IMMEDIATE acute renal failure: because the ACE works on the efferent arteriole: making the pt. rely on the afferent: but if the afferent is injured: these ACE’s wont work
- ^^^ more seen in bilateral renal artery stenosis
Renal Artery Stenosis
Diagnosis
Treatment
Diagnosis
- elevated BUN & Cr.
- use US (hard with increase adipose tissue)
- use CT aniography, MRA
- gold standard dx.: renal angiography
Treatment
- medications to control the HTN
- angioplasty with or without stent
- surgical bypass
- fibromuscular : angioplasty without a stent is good
- stening = bypass in terms of outcomes
Renal Vein Thrombosis
Etiology
Presentation
Etiology
- a thrombotic occulsion of 1 or both of the renal veins, resulting in AKI or CKD
- LEFT renal vein more common
- 2/3 of cases are bilateral: this is because if you have a thromobosis probelm its usually systemic
Causes
- nephrotic synrome (membranous nephropathy) = hypercoaguable state = increased clot formation
- other hypercoaguable disorders
- tumors & malignancy
- medications (OCPs)
Presentation
- flank pain
- tenderness
- hematuria
- rapid decline in renal function
- proteinuria
Renal Vein Thrombosis
Diagnosis
Treatment
Diagnosis
- doppler US
- CTA (100% sensitive)
- MRA ($$)
Treatment
- anticoag. thearpy & treat underlying
- endovascualr thrombolysis (injection) can be considerd in severe cases
- IVC filter if needed to prevent migration
Simple Renal Cyst
- where found
- US findings
- follow/treat
majority of the renal masses found: are a simple cyst
found incidentally on US in the outer cortex
US findings
- echo free (dark)
- sharply demarcated walls that a re smooth
- the light will go through it: see a back wall transmission because its fluid!
Follow
- benign cyst doesnt need follow up – if it hcanges, taht warrents investigation
Polycystic Kidney Disease
Etiology
Presentation
Etiology
- can be most common life threatening inherited disease worldwide
two types: dominant and resessive
Autosomal Dominant PKD (ADPKD) : adults with later onset finding (4th or 5th decade)
- a mutation in the PKD-1 (C16) or PKD-2 (C4)
- cysts accumulate fluid, grow, compress the kidney & significantly impact renal function
Autosomal Recessive PKD (ARPKD) : children found early onset
- seen in childhood
- 50% of neonates die due to disease
- not many survive past 10
- the enlarged kidneys grow so fast it impacts function early on –> metablic acidosis & HTN early in life
Polycystic Kidney Disease
Etiology
Presentation
Etiology
- can be most common life threatening inherited disease worldwide
two types: dominant and resessive
Autosomal Dominant PKD (ADPKD) : adults with later onset finding (4th or 5th decade)
- a mutation in the **PKD-1 (C16) or PKD-2 (C4) **
- cysts accumulate fluid, grow, compress the kidney & significantly impact renal function
Autosomal Recessive PKD (ARPKD) : children found early onset
- seen in childhood
- 50% of neonates die due to disease
- not many survive past 10
- the enlarged kidneys grow so fast it impacts function early on –> metablic acidosis & HTN early in life
